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1.
J Neuroendovasc Ther ; 16(1): 56-62, 2022.
Article in English | MEDLINE | ID: mdl-37502025

ABSTRACT

Objective: We treated a case of scalp arteriovenous malformation (sAVM) by transvenous embolization using Onyx. Case Presentation: We describe the case of a 17-year-old woman with a pulsatile mass at the right temporal area. DSA identified sAVM with the venous pouch between the right occipital artery (OA) and the right two occipital veins (OVs), which was also fed by multiple branches of the right posterior auricular artery (PAA) and superficial temporal artery (STA). The shunts were completely occluded by the reverse pressure cooker technique (RPCT), which involves navigating the balloon catheters just distal to the shunt point in the OVs approaching from the right external jugular vein (EJV) and injecting Onyx to each feeder retrogradely with balloons inflated. Conclusion: This technique may be useful for treating sAVM with venous angioarchitecture enabling a transvenous approach.

2.
J Appl Physiol (1985) ; 103(5): 1669-77, 2007 Nov.
Article in English | MEDLINE | ID: mdl-17761788

ABSTRACT

Heart rate (HR) is controlled solely by via cardiac parasympathetic outflow in tetraplegic individuals, who lack supraspinal control of sympathetic outflows and circulating catecholamines but have intact vagal pathways. A high-frequency component (HF; at 0.15-0.40 Hz) of the power spectrum of HR variability and its relative value against total power (HF/Total) were assessed using a wavelet transform to identify cardiac parasympathetic outflow. The relative contribution of cardiac parasympathetic and sympathetic outflows to controlling HR was estimated by comparing the HF/Total-HR relationship between age-matched tetraplegic and normal men. Six tetraplegic men with complete cervical spinal cord injury performed static arm exercise at 35% of the maximal voluntary contraction until exhaustion. Although resting cardiac output and arterial blood pressure were lower in tetraplegic than normal subjects, HR, HF, and HF/Total were not statistically different between the two groups. When tetraplegic subjects developed the same force during exercise as normal subjects, HF and HF/Total decreased to 67-90% of the preexercise control and gradually recovered 1.5 min after exercise. The amount and time course of the changes in HF/Total during and after exercise coincided well between both groups. In contrast, the increase in HR at the start of exercise was blunted in tetraplegic compared with normal subjects, and the HR recovery following exercise was also delayed. It is likely that, although the withdrawal response of cardiac parasympathetic outflow is preserved in tetraplegic subjects, sympathetic decentralization impairs the rapid acceleration of HR at the onset of exercise and the rapid deceleration following exercise.


Subject(s)
Exercise , Heart Rate , Heart/innervation , Muscle Contraction , Muscle, Skeletal/physiopathology , Parasympathetic Nervous System/physiopathology , Quadriplegia/physiopathology , Spinal Cord Injuries/complications , Adaptation, Physiological , Adult , Blood Pressure , Cardiac Output , Case-Control Studies , Humans , Male , Models, Cardiovascular , Physical Endurance , Quadriplegia/etiology , Research Design , Spinal Cord Injuries/physiopathology , Sympathetic Nervous System/physiopathology , Time Factors , Vagus Nerve/physiopathology
3.
J Appl Physiol (1985) ; 97(6): 2077-82, 2004 Dec.
Article in English | MEDLINE | ID: mdl-15310746

ABSTRACT

The purpose of the present study was 1) to investigate whether an increase in heart rate (HR) at the onset of voluntary static arm exercise in tetraplegic subjects was similar to that of normal subjects and 2) to identify how the cardiovascular adaptation during static exercise was disturbed by sympathetic decentralization. Mean arterial blood pressure (MAP) and HR were noninvasively recorded during static arm exercise at 35% of maximal voluntary contraction in six tetraplegic subjects who had complete cervical spinal cord injury (C(6)-C(7)). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were estimated by using a Modelflow method simulating aortic input impedance from arterial blood pressure waveform. In tetraplegic subjects, the increase in HR at the onset of static exercise was blunted compared with age-matched control subjects, whereas the peak increase in HR at the end of exercise was similar between the two groups. CO increased during exercise with no or slight decrease in SV. MAP increased approximately one-third above the control pressor response but TPR did not rise at all throughout static exercise, indicating that the slight pressor response is determined by the increase in CO. We conclude that the cardiovascular adaptation during voluntary static arm exercise in tetraplegic subjects is mainly accomplished by increasing cardiac pump output according to the tachycardia, which is controlled by cardiac vagal outflow, and that sympathetic decentralization causes both absent peripheral vasoconstriction and a decreased capacity to increase HR, especially at the onset of exercise.


Subject(s)
Adaptation, Physiological/physiology , Blood Pressure/physiology , Exercise/physiology , Heart Rate/physiology , Quadriplegia/physiopathology , Adult , Arm/physiology , Humans , Male , Physical Endurance/physiology , Stroke Volume/physiology , Sympathetic Nervous System/physiology , Vagus Nerve/physiology , Vasoconstriction/physiology , Volition/physiology
4.
Mol Cancer Ther ; 2(11): 1139-47, 2003 Nov.
Article in English | MEDLINE | ID: mdl-14617787

ABSTRACT

Angiotensin II (A-II) receptor (AT(1) receptor) blockers (ARB) are a class of antihypertensive agent. It is known that they suppress signal transduction pathways mediated by growth factors [e.g., epidermal growth factor (EGF)] through the AT(1) receptor in vascular endothelial cells. In the present study, we demonstrated that A-II activates the cell proliferation of prostate cancer as well as EGF. In addition, we showed that A-II induces the phosphorylations of mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription 3 (STAT3) in prostate cancer cells. In contrast, ARB was shown to inhibit the proliferation of prostate cancer cells stimulated with EGF or A-II, the mechanism of which is through the suppression of MAPK or STAT3 phosphorylation by ARB. Oral administration of ARB to nude mice inhibited the growth of prostate cancer xenografts in both androgen-dependent and androgen-independent cells in a dose-dependent manner. Microvessel density was reduced in xenografts treated with ARB, which means ARB inhibits the vascularization of xenografts. Expression of AT(1) receptor mRNA was examined by reverse transcription-PCR using 10 pairs of human prostate cancer and normal prostate tissues. AT(1) receptor expression in human prostate cancer tissue was higher (9 of 10 cases) than that in normal prostate tissue. These results suggest the possibility that ARB is a novel therapeutic class of agents for prostate cancer, especially hormone-independent tumors.


Subject(s)
Angiotensin II/antagonists & inhibitors , Angiotensin Receptor Antagonists , Antineoplastic Agents/pharmacology , Epidermal Growth Factor/antagonists & inhibitors , Prostatic Neoplasms/pathology , Protein-Tyrosine Kinases/antagonists & inhibitors , Adenocarcinoma/pathology , Angiotensin II/pharmacology , Animals , Cell Division/drug effects , DNA-Binding Proteins/metabolism , Epidermal Growth Factor/pharmacology , Humans , Male , Mice , Mice, Nude , Mitogen-Activated Protein Kinases/metabolism , Neoplasm Transplantation , Phosphorylation/drug effects , Protein-Tyrosine Kinases/metabolism , Receptors, Angiotensin/genetics , Receptors, Angiotensin/metabolism , STAT3 Transcription Factor , Signal Transduction/drug effects , Trans-Activators/metabolism , Tumor Cells, Cultured
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